Figure 2: Impaired immunorecognition of tumour cells during checkpoint blockade immunotherapy(A) Defects in the tumour antigen processing and presentation machinery can render a tumour cell invisible to tumour-specific CD8 T cells. (B) During a therapy-elicitedimmune response, cancer cells that express specific peptide MHCs are selectively culled by antigen-specific T cells. Interferon-γ released by immune effector cells mightexpedite this immunoediting process. As a result, tumour clones emerge that do not bear the original cognate antigens required for productive immune recognition.(C) Decreased abundance and diversity of intratumoural activated CD8 T cells, which might result from deregulation of naive T-cell priming and proliferation, can allowtumours to escape anticancer immunosurveillance.
HLA=human leucocyte antigen. B2M=β-2-microglobulin. CANX=calnexin. HSPA5=heat shock 70 kDa protein 5.TAP=transporter associated with antigen processing. TAPBP=transporter associated with antigen processing binding protein. CALR=calreticulin. PDIA3=proteindisulfide-isomerase A3. TCR=T-cell receptor. ER=endoplasmic reticulum.
HLA=human leucocyte antigen. B2M=β-2-microglobulin. CANX=calnexin. HSPA5=heat shock 70 kDa protein 5.TAP=transporter associated with antigen processing. TAPBP=transporter associated with antigen processing binding protein. CALR=calreticulin. PDIA3=proteindisulfide-isomerase A3. TCR=T-cell receptor. ER=endoplasmic reticulum.